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Article: A rat model of thyroid hormone-induced bone loss: Effect of antiresorptive agents on regional bone density and osteocalcin gene expression

TitleA rat model of thyroid hormone-induced bone loss: Effect of antiresorptive agents on regional bone density and osteocalcin gene expression
Authors
Issue Date1994
PublisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/thy
Citation
Thyroid, 1994, v. 4 n. 1, p. 93-98 How to Cite?
AbstractThyroid hormone has been shown to stimulate bone resorption. Both endogenous hyperthyroidism and exogenous thyroxine suppressive therapy have been associated with reduction in bone mineral density (BMD), but the patholophysiology of thyroxine-induced bone loss is not well understood. First we studied the effect of L-T4 (0.1-0.3 μg/g body weight ip/day) on bone turnover in rats by measuring regional BMDs and osteocalcin mRNA. Next we determined whether antiresorptive agents (calcitonin 1 μU/g ip/day or sodium etidronate given cyclically at 10 μg/g po for 3 consecutive days out of every week) could prevent bone loss. Groups of 10 male Sprague-Dawley rats each weighing 320-350 g were studied before and after 3 weeks of treatment. L-T4 treatment resulted in reduction in BMDs in the lumbar spine, tail, and femur as measured by dual energy X-ray absorptiometry, but there was no correlation with the dosage of L-T4 or the serum T4 level. Treatment with sodium etidronate or calcitonin alone did not alter the regional BMD. Cyclical sodium etidronate, but not calcitonin, was able to prevent the bone loss induced by L-T4 treatment. L-T4 caused a dose-dependent increase in femur osteocalcin mRNA concentration. Treatment with calcitonin resulted in 50% reduction of osteocalcin mRNA, but sodium etidronate had no effect. In conclusion, cyclical sodium etidronate prevents bone loss induced by exogenous L-T4 in rats and may be useful in preventing osteoporosis in patients given long term TSH-suppressive doses of thyroxine therapy.
Persistent Identifierhttp://hdl.handle.net/10722/162054
ISSN
2015 Impact Factor: 3.784
2015 SCImago Journal Rankings: 1.458
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKung, AWCen_US
dc.contributor.authorNg, Fen_US
dc.date.accessioned2012-09-05T05:16:55Z-
dc.date.available2012-09-05T05:16:55Z-
dc.date.issued1994en_US
dc.identifier.citationThyroid, 1994, v. 4 n. 1, p. 93-98en_US
dc.identifier.issn1050-7256en_US
dc.identifier.urihttp://hdl.handle.net/10722/162054-
dc.description.abstractThyroid hormone has been shown to stimulate bone resorption. Both endogenous hyperthyroidism and exogenous thyroxine suppressive therapy have been associated with reduction in bone mineral density (BMD), but the patholophysiology of thyroxine-induced bone loss is not well understood. First we studied the effect of L-T4 (0.1-0.3 μg/g body weight ip/day) on bone turnover in rats by measuring regional BMDs and osteocalcin mRNA. Next we determined whether antiresorptive agents (calcitonin 1 μU/g ip/day or sodium etidronate given cyclically at 10 μg/g po for 3 consecutive days out of every week) could prevent bone loss. Groups of 10 male Sprague-Dawley rats each weighing 320-350 g were studied before and after 3 weeks of treatment. L-T4 treatment resulted in reduction in BMDs in the lumbar spine, tail, and femur as measured by dual energy X-ray absorptiometry, but there was no correlation with the dosage of L-T4 or the serum T4 level. Treatment with sodium etidronate or calcitonin alone did not alter the regional BMD. Cyclical sodium etidronate, but not calcitonin, was able to prevent the bone loss induced by L-T4 treatment. L-T4 caused a dose-dependent increase in femur osteocalcin mRNA concentration. Treatment with calcitonin resulted in 50% reduction of osteocalcin mRNA, but sodium etidronate had no effect. In conclusion, cyclical sodium etidronate prevents bone loss induced by exogenous L-T4 in rats and may be useful in preventing osteoporosis in patients given long term TSH-suppressive doses of thyroxine therapy.en_US
dc.languageengen_US
dc.publisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/thyen_US
dc.relation.ispartofThyroiden_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThis is a copy of an article published in the [Thyroid] © [1994] [copyright Mary Ann Liebert, Inc.]; [Thyroid] is available online at: http://www.liebertonline.com-
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshBone Density - Drug Effectsen_US
dc.subject.meshBone Resorption - Chemically Induced - Genetics - Prevention & Controlen_US
dc.subject.meshCalcitonin - Pharmacologyen_US
dc.subject.meshDna, Complementary - Geneticsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEtidronic Acid - Pharmacologyen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshOsteocalcin - Geneticsen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshThyroxine - Blood - Pharmacologyen_US
dc.titleA rat model of thyroid hormone-induced bone loss: Effect of antiresorptive agents on regional bone density and osteocalcin gene expressionen_US
dc.typeArticleen_US
dc.identifier.emailKung, AWC:awckung@hku.hken_US
dc.identifier.authorityKung, AWC=rp00368en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1089/thy.1994.4.93-
dc.identifier.pmid8054866-
dc.identifier.scopuseid_2-s2.0-0028350050en_US
dc.identifier.volume4en_US
dc.identifier.issue1en_US
dc.identifier.spage93en_US
dc.identifier.epage98en_US
dc.identifier.isiWOS:A1994NJ42500019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKung, AWC=7102322339en_US
dc.identifier.scopusauthoridNg, F=37004123900en_US

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